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Infectious bursal disease is an acute, immunosuppressive infectious disease in chickens caused by the infectious bursal disease virus (IBDV), which causes huge economic losses to the global poultry industry. Persistently circulating very virulent IBDV (vvIBDV) and newly emerging novel variant IBDV (nVarIBDV) are the two dominant epidemic strains of IBDV in East Asian countries such as China. Compared to lethal vvIBDV, nonlethal nVarIBDV has more insidious pathogenicity and can partially escape the immune protection of the existing vvIBDV vaccine, suggesting its potential adaptive survival strategy. However, the underlying molecular mechanism remains unknown. The viral capsid protein VP2 is closely related to cell tropism, virulence, and antigenic variation of IBDV. In this study, for the first time, we demonstrated that residue 279 of VP2 is responsible for the difference in pathogenicity between nVarIBDV and vvIBDV and that the D279N substitution reduces the lethality of vvIBDV from 70% to 0%. Moreover, a significant reduction in the viral load and inflammatory factor levels in the immune organs and blood of infected chickens may be important mechanisms for reducing the lethality of IBDV. Additionally, residue 279 was an important molecular basis for the antigenic differences between nVarIBDV and vvIBDV. D279N substitution reduced the neutralizing ability of vvIBDV antiserum against nVarIBDV by affecting the binding ability of antibodies and antigens. Our results indicate that nVarIBDV has an infection transmission strategy that facilitates its survival by hiding viral pathogenicity and escaping antiserum neutralization, which not only has significant implications for the systemic cognition of viral genetic evolution and pathogenesis but also provides new ideas for the comprehensive prevention and control of IBDV. [ABSTRACT FROM AUTHOR]